Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice

Hu, Chengyun; Dai, Feibiao; Wang, Jiawu; Jiang, Lai; Wang, Di; Gao, Jie; Huang, Jun; Luo, Jianfeng; Tang, Fei; Zhang, Zhetao; Tang, Chaoliang

doi:10.1155/2022/5067544

Cited by 6 publications

(3 citation statements)

References 46 publications

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“…Hu C. et al described that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown accelerated pressure overload-induced cardiac hypertrophy and dysfunction in mice by activating oxidative stress and cardiomyocyte apoptosis [ 31 ]. Kunze A et al reported on decreased Prdx5 levels in severe stroke [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Selenoprotein P, Peroxiredoxin-5, Renalase and Selected Cardiovascular Consequences Tested in Ambulatory Blood Pressure Monitoring and Echocardiography

et al. 2023

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This study aimed to assess the relationship between chosen antioxidants, namely selenoprotein P (SELENOP), peroxiredoxin-5 (Prdx-5), renalase and selected cardiovascular consequences tested in ambulatory blood pressure monitoring (ABPM) and echocardiography (ECHO). In our work, cardiovascular consequences refer to higher mean blood pressure (MBP) and pulse pressure (PP) on ABPM, as well as to left atrial enlargement (LAE), left ventricular hypertrophy (LVH) and lower left ventricular ejection fraction (LVEF%) on ECHO. The study group consisted of 101 consecutive patients admitted to the Department of Internal Medicine, Occupational Diseases and Hypertension to verify the diagnosis of Obstructive Sleep Apnoea (OSA). Each patient underwent full polysomnography, blood tests, ABPM and ECHO. Both selenoprotein-P and renalase levels correlated with different ABPM and ECHO parameters. We found no correlation between the peroxiredoxin-5 level and none of the tested parameters. We point to the possible application of SELENOP plasma-level testing in the initial selection of high cardiovascular-risk patients, especially if access to more advanced examinations is limited. We further suggest SELENOP measurement as a possible indicator of patients at increased left ventricular hypertrophy risk who should be of particular interest and may benefit from ECHO testing.

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Section: Discussionmentioning

confidence: 99%

Selenoprotein P, Peroxiredoxin-5, Renalase and Selected Cardiovascular Consequences Tested in Ambulatory Blood Pressure Monitoring and Echocardiography

et al. 2023

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“…Due to the long-term effect of pre-and post-cardiac overload, hypertrophic cardiomyocytes are more sensitive to oxidative damage caused by ischemia, hypoxia and ROS, and are superimposed on inflammatory factors, high levels of Ca 2+ , NO and other stimulatory factors, resulting in an increase in cytoplasmic density and cell membrane permeability, nuclear pyknosis and fragmentation, and DNA degradation, leading to the occurrence of cardiomyocyte apoptosis (Hu et al, 2022). In this paper, the apoptosis of cardiomyocytes was observed by flow cytometry, and it was found that GXN had a certain inhibitory effect on the apoptosis process in hypertrophic cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Guanxinning tablets improve myocardial hypertrophy by inhibiting the activation of MEK-ERK1/2 signaling pathway

Zhang,

Huang,

et al. 2023

JAB

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Myocardial hypertrophy may lead to heart failure and sudden death. As traditional Chinese medicine, Guanxinning tablets (GXN) have significant pharmacological effects in the prevention and treatment of cardiovascular diseases. However, the anti-cardiac hypertrophy efficacy of GXN and its mechanism of action are still unclear. Therefore, we established a heart failure rat model and isolated primary cardiomyocytes of neonatal rat to observe the protective effect of GXN on heart failure rat model and the intervention effect on myocardial cell hypertrophy, and to explore the possible mechanism of GXN preventing and treating myocardial hypertrophy. The results of in vivo experiments showed that GXN could significantly reduce the degree of cardiac hypertrophy, reduce the size of cardiomyocytes, inhibit the degree of myocardial remodeling and fibrosis, and improve cardiac function in rats with early heart failure. The results of in vitro experiments showed that GXN was safe for primary cardiomyocytes and could improve cardiomyocyte hypertrophy and reduce the apoptosis of cardiomyocytes in pathological state, which may be related to the inhibition of the over-activation of MEK-ERK1/2 signaling pathway. In conclusion, GXN may inhibit cardiac hypertrophy and improve early heart failure by inhibiting the over-activation of MEK-ERK1/2 signaling pathway.

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“…DUSPs regulate the downstream effectors (ERK, JNK and p38) of MAPK signaling pathway through dephosphorylating the upstream MAPK molecules, such as ASK1, TAK1, and MEK [24]. Accumulating data suggest that the over-activated MAPK signaling pathway promotes the pathological progress of myocardial hypertrophy [25]. Thus, DUSPs might control cardiac remodeling induced by the pathological stimulus through negatively regulating MAPK signaling cascades.…”

Section: Discussionmentioning

confidence: 99%

Dual-Specificity Phosphatase 19 Alleviates Cardiac Hypertrophy Via Inhibiting ASK1 Phosphorylation

Jia

Liu

et al. 2022

SSRN Journal

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Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice

Cited by 6 publications

References 46 publications

Selenoprotein P, Peroxiredoxin-5, Renalase and Selected Cardiovascular Consequences Tested in Ambulatory Blood Pressure Monitoring and Echocardiography

Selenoprotein P, Peroxiredoxin-5, Renalase and Selected Cardiovascular Consequences Tested in Ambulatory Blood Pressure Monitoring and Echocardiography

Guanxinning tablets improve myocardial hypertrophy by inhibiting the activation of MEK-ERK1/2 signaling pathway

Dual-Specificity Phosphatase 19 Alleviates Cardiac Hypertrophy Via Inhibiting ASK1 Phosphorylation

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